Hodgkin's disease of bone marrow masquerading as a heavy plasma cell infiltration and fibrosis
Version of Record online: 23 JUL 2003
British Journal of Haematology
Volume 122, Issue 3, page 343, August 2003
How to Cite
Joshi, A. and Aqel, N. M. (2003), Hodgkin's disease of bone marrow masquerading as a heavy plasma cell infiltration and fibrosis. British Journal of Haematology, 122: 343. doi: 10.1046/j.1365-2141.2003.04405.x
- Issue online: 23 JUL 2003
- Version of Record online: 23 JUL 2003
A 62-year-old female patient presented with enlargement of multiple cervical lymph nodes for which she underwent lymph node biopsy, bone marrow trephine biopsy and marrow aspiration. The trephine biopsy showed two marrow spaces filled with sheets of plasma cells (top left) with associated grade three reticulin deposition. While the appearances were suggestive of multiple myeloma, other spaces showed reticulin fibrosis with infiltration by small lymphocytes and histiocytes (top right). The diagnosis became obvious when the lymph node biopsy was examined. This showed the cellular phase of nodular sclerosing Hodgkin's disease with numerous CD30-positive, CD15-positive Reed–Sternberg cells (bottom). Most of the lymph node's background cells were mature plasma cells occurring in sheets and surrounding nodules of Reed–Sternberg cells. The marrow biopsy was re-interpreted as showing probable involvement by Hodgkin's disease, but no Reed–Sternberg cells or mononuclear Hodgkin's cells could be demonstrated on multiple levels or on CD30 immunostaining.
This case highlights the following points:
(1) Marrow involvement in Hodgkin's disease should be part of the differential diagnosis of marrow fibrosis especially when associated with the inflammatory cell infiltration normally seen in Hodgkin's disease. In patients with known Hodgkin's disease, the finding of marrow fibrosis should encourage the search for diagnostic Reed–Sternberg cells and multiple levels of bone marrow trephine biopsies should be examined and complemented by immunostaining for CD30. However, diagnosis of marrow involvement in Hodgkin's disease can be suspected in the absence of Reed–Sternberg cells, as seen in our case. This can be based on the presence of marrow fibrosis associated with inflammatory cells seen normally in Hodgkin's disease (i.e. lymphocytes, histiocytes, mature eosinophils and plasma cells), as has been outlined in the original recommendations of the Ann Arbor symposium. However, the presence of Reed–Sternberg or mononuclear Hodgkin's cells is essential to establish a definite marrow involvement by Hodgkin's disease.
(2) Marrow plasmacytosis is recognized in Hodgkin's disease. Our case represents an extreme example in which some marrow spaces were completely replaced by plasma cells. Such a finding could lead to a misdiagnosis of myeloma in a small non-representative biopsy.